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Alcohol Alcohol. 2011 Sep-Oct;46(5):514-22. doi: 10.1093/alcalc/agr063. Epub 2011 Jun 17.

Combined pre- and postnatal ethanol exposure in rats disturbs the myelination of optic axons.

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  • 1Ophthalmic Research Unit Santiago Grisolía, University Hospital Dr Peset, Av Gaspar Aguilar 90, 46017 Valencia, Spain.

Erratum in

  • Alcohol Alcohol. 2012 May-Jun;47(3):225.



To analyse myelination and outgrowth of the optic axons in relation to the neuro-ophthalmological manifestations of ethanol (EtOH) abuse during pregnancy.


An experimental model of chronic EtOH exposure was developed in rats and their offspring by subjecting the dams to a liquid diet (35% of the daily total calories as either EtOH or maltose-dextrose nutritional controls (Con). Eyeballs and optic nerves were obtained at key developmental stages and processed for morphologic, immunocytochemical and immunoblotting procedures, using alternatively antibodies against myelin basic protein (MBP) or neurofilament (NF) protein, and image analysing.


A significant delay in onset of optic axons myelination, as well as a significant reduction in optic nerve size (P < 0.001), optic axons number (P < 0.001), myelinated axons density (P < 0.001), number of myelin lamellae linked to axon diameter (P < 0.001) and optic axon cross-sectional area (P < 0.001) were detected in the global morphometric assessment of the EtOH nerves with respect to the Con. Expression of MBP and NF was noticeably reduced in the EtOH optic nerves when compared with the Con.


Disturbed myelination of optic axons, caused by EtOH abuse, strongly disrupts the optic nerve development and the establishment of definitive retinal and optic nerve targets, and subsequently the visual patterns.

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